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Necrosis in distal areas of random skin flaps remains a challenging issue. Curculigoside A (CA), one of the main bioactive phenolic compounds, has been reported to induce angiogenesis in vitro by increasing proliferation, tube formation, and migration. In addition, CA was shown to increase vascular endothelial growth factor (VEGF) expression. In this study, we investigated the potential use of CA as a novel candidate to enhance the viability of the ischemic skin flap. A modified McFarlane flap was used as a surgical model in Sprague-Dawley rats. Three groups of rats were treated as follows: the control group received 0.9% saline orally, while rats in the two treatment groups were administered 10mg/kg or 20mg/kg CA orally for 7 days, respectively. On day7, the mice were killed, and tissue samples were collected for hematoxylin and eosin staining and immunohistochemical examination, while laser Doppler imaging and oxide-gelatin angiography were performed to assess angiogenesis. Kits for the analysis of superoxide dismutase (SOD) and malondialdehyde (MDA) were used to verify the oxidative stress level. Treating animals with CA significantly increased the surviving portion of the flaps. VEGF and SOD expression and microvessel development were markedly increased, and the MDA level was reduced, in the CA treatment groups. Histological studies demonstrated that CA promoted angiogenesis and attenuated inflammatory cell numbers. These findings indicated that CA increases random skin flap survival.